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• W2000604813 abstract "Two-pore domain K(+) (K2P) channels are involved in a variety of physiological processes by virtue of their high basal activity and sensitivity to various biological stimuli. One of these processes is secretion of hormones and transmitters in response to stimuli such as hypoxia, acidosis, and receptor agonists. The rise in intracellular [Ca(2+)] ([Ca(2+)]i) that is critical for the secretory event can be achieved by several mechanisms: (a) inhibition of resting (background) K(+) channels, (b) activation of Na(+)/Ca(2+)-permeable channels, and (c) release of Ca(2+) from intracellular stores. Here, we discuss the role of TASK and TREK in stimulus-secretion mechanisms in carotid body chemoreceptor cells and adrenal medullary/cortical cells. Studies show that stimuli such as hypoxia and acidosis cause cell depolarization and transmitter/hormone secretion by inhibition of TASK or TREK. Subsequent elevation of [Ca(2+)]i produced by opening of voltage-dependent Ca(2+) channels then activates a Na(+)-permeable cation channel, presumably to help sustain the depolarization and [Ca(2+)]i. Agonists such as angiotensin II may elevate [Ca(2+)]i via multiple mechanisms involving both inhibition of TASK/TREK and Ca(2+) release from internal stores to cause aldosterone secretion. Thus, inhibition of resting (background) K(+) channels and subsequent activation of voltage-gated Ca(2+) channels and Na(+)-permeable non-selective cation channels may be a common ionic mechanism that lead to hormone and transmitter secretion." @default.
• W2000604813 created "2016-06-24" @default.
• W2000604813 creator A5002369637 @default.
• W2000604813 creator A5060181991 @default.
• W2000604813 date "2014-12-06" @default.
• W2000604813 modified "2023-09-26" @default.
• W2000604813 title "Role of K2P channels in stimulus-secretion coupling" @default.
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• W2000604813 doi "https://doi.org/10.1007/s00424-014-1663-3" @default.
• W2000604813 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4400227" @default.
• W2000604813 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/25476848" @default.
• W2000604813 hasPublicationYear "2014" @default.
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